An adult human weighing 70 kg, with average physical activity, requires about 2400-2900 kcal from metabolic fuels each day to maintain basal metabolic functions. The requirement for metabolic fuels is generally constant throughout the day. However, if the intake of carbohydrates is lower than energy expenditures, such as may be the case during intense or prolonged physical activity, glucose derived from ingested carbohydrates is spared for use by the central nervous system and erythrocytes, and glycogen stores are mobilized to provide energy to muscle tissue.
Glycogen is the major storage carbohydrate in mammals and is a branched polymer of α-D-glucose. It occurs mainly in the liver and muscle tissue, with a proportionately greater amount occurring in muscle tissue because of its greater overall mass in the body. In the liver, glycogen's major function is to provide glucose for extrahepatic tissues. In muscles, it serves mainly as a ready source of metabolic fuel.
Glycogen is synthesized from glucose by the pathway of glycogenesis and is broken down into glucose-6-phosphate and, ultimately, glucose by a separate pathway known glycogenolysis. Glycogenolysis leads to glucose formation in the liver and lactate formation in muscle owing to the respective presence or absence of glucose-6-phosphatase. Cyclic adenosine monophosphate (cAMP) integrates the regulation of glycogenolysis and glycogenesis by promoting simultaneous activation of phosphorylase and inhibition of glycogen synthase.
Glucose uptake into the muscle tissue is controlled by insulin which is secreted by the B islet cells of the pancreas in response to an increased concentration in the portal blood. An early response to insulin in muscle tissue is the migration of glucose transporter vehicles to the cell surfaces, exposing active glucose transporters (GLUT 4). These insulin-sensitive tissues will generally only take up glucose from the blood stream in any significant extent in the presence of insulin. As insulin secretion falls, the transporters are internalized again reducing glucose uptake.
Insulin acts reciprocally by inhibiting glycogenolysis and stimulating glycogenesis. Insulin is secreted in direct response to high blood glucose levels and stimulates the liver to store glucose as glycogen (glycogenesis). As blood glucose levels fall glucagon secretion by the pancreas increases stimulating the break down of glycogen into glucose (glycogenolysis). Large intakes of carbohydrates about 30-60 minutes prior to exercise may have a detrimental effect on performance by causing an elevation of insulin pushing glucose into the cells and consequently inhibition of fatty acid mobilization. If less fat is available to the muscles, the limited glycogen stores will be used at a faster rate, thus hastening the onset of fatigue. During exercise, insulin secretion is inhibited, thus the ingestion of carbohydrates during exercise does not inhibit fat mobilization and may improve performance. However, the lack of insulin promotes glycogenolysis or the depletion of glycogen stores which can lead to fatigue.
The hallmarks of insulin action are the stimulation of anabolic responses and suppression of catabolic responses. These responses are orchestrated by the insulin pathway and are initiated by the binding of insulin to the insulin receptor. In patients with diabetes mellitus the body either does not produce insulin (Type I) or the body cannot use insulin properly (Type II) with insulin resistance playing a key role in the development of the disease. Symptoms of insulin resistance include a decreased stimulation of muscle glycogen synthesis (glycogenesis) and defects in glycogen synthase activity, hexokinase activity, and glucose uptake.
Generally, physical training enhances insulin-stimulated glucose disposal in proportion to the improvement in physical fitness. Further, athletes are typically more sensitive to insulin. Thus, even with ingestion of small amount of simple carbohydrates, athletes can experience a spike in insulin secretion which can speed the depletion of glucose in the blood stream which in turn signals the reduction in insulin production. However, as noted above, once blood glucose levels begin to fall, glucose is spared for use by the central nervous system and erythrocytes, while skeletal tissue turns to glycogen stores and glycogenolysis.
Accordingly, there is a need and/or a desire for a method of enhancing muscle performance which provides both a supply of glucose to muscle tissue at the start of exercise or athletic activity and a steady supply of glucose to muscle tissues during physical activity to promote glycogen conservation, storage, and/or resynthesis and which avoids or offsets the consequences of insulin spikes resulting from the ingestion of carbohydrates and/or the inhibition of insulin production during physical activity.